PURPOSE: The aim of this experimental study was to evaluate the potential of a simple expiration technique by means of magnetic resonance imaging (MRI) in an animal model to detect pulmonary air-trapping areas after artificial bronchial obstruction. MATERIAL AND METHODS: Sixteen pigs were evaluated by means of a modified T1-weighted FLASH with fat saturation in respiratory arrest (TR=4.6 ms, TE=1.8 ms, alpha=10 degrees, S.D.=3-5 mm). A measurement of the signal intensity (SI) in the peripheral lung tissue was made in both inspiration and expiration before and after inhalation of 2 ml of 0.5% acetylcholine to simulate a bronchial obstruction. A final measurement of the lung SI was also made after bronchospasmolytic induction through salbutamol (beta2-mimetic bronchodilator). RESULTS: In expiration, a mean SI increase in peripheral lung tissue of about 183% was seen in comparison to inspiration (mean SI increase of 11-32). After inhalation of 0.5% acetylcholine, the expirational signal increase in peripheral lung tissue was only 114% of the original SI. The expirational signal homogeneity decreased after inhalation of acetylcholine. After inhalation of salbutamol, the lung tissue signal elevation in expiration was 193%. CONCLUSION: We interpret the low expiratory signal elevation after acetylcholine inhalation as a result of an air-trapped bronchial constriction in certain areas. The simple expiratory technique in an animal model showed that it is suitable to demonstrate obstructive air trapping using MRI.
PURPOSE: The aim of this experimental study was to evaluate the potential of a simple expiration technique by means of magnetic resonance imaging (MRI) in an animal model to detect pulmonary air-trapping areas after artificial bronchial obstruction. MATERIAL AND METHODS: Sixteen pigs were evaluated by means of a modified T1-weighted FLASH with fat saturation in respiratory arrest (TR=4.6 ms, TE=1.8 ms, alpha=10 degrees, S.D.=3-5 mm). A measurement of the signal intensity (SI) in the peripheral lung tissue was made in both inspiration and expiration before and after inhalation of 2 ml of 0.5% acetylcholine to simulate a bronchial obstruction. A final measurement of the lung SI was also made after bronchospasmolytic induction through salbutamol (beta2-mimetic bronchodilator). RESULTS: In expiration, a mean SI increase in peripheral lung tissue of about 183% was seen in comparison to inspiration (mean SI increase of 11-32). After inhalation of 0.5% acetylcholine, the expirational signal increase in peripheral lung tissue was only 114% of the original SI. The expirational signal homogeneity decreased after inhalation of acetylcholine. After inhalation of salbutamol, the lung tissue signal elevation in expiration was 193%. CONCLUSION: We interpret the low expiratory signal elevation after acetylcholine inhalation as a result of an air-trapped bronchial constriction in certain areas. The simple expiratory technique in an animal model showed that it is suitable to demonstrate obstructive air trapping using MRI.